山梨医科大学雑誌　第7巻1号　011-017(1992)

Loss of Heterozygosity at the HP Locus on Chromosome 16 in
Hepatocellular Carcinoma

Masanori MATSUDA

Abstract: Loss of heterozygosity (LOH) on chromosome 16 has been reported in human hepatocellular carcinoma (HCC); putative recessive oncogenes are thought to be contained in the deleted regions.
In this study, we used Southern blot hybridization to examine LOH at the HP locus on chromosome 16 in 28 primary HCC lesions of 24 patients. These lesions consisted of 3 multicentric lesions and one recurrent main lesion, 3 intra- and one extrahepatic metastases, one portal vein embolus, and 24 non-cancerous liver tissue specimens from the 24 patients. Constitutional heterozygosity at the HP locus was detected in 9 of the 24 patients (44.4%), in 15 lesions. Of the 10 informative main lesions (9 primary lesions and one recurrent main lesion), 5 lesions (50.0%); 4 primary lesions from 4 cases, and the recurrent main lesion from another case, showed LOH at the HP locus. The primary lesion of the recurrent case (resected 4 years previously) did not show LOH, but all recurrent tumors, including metastases which were confirmed to be metastatic tumors of the primary HCC lesion, showed LOH. No deletion at the HP locus was detected in any informative non-cancerous liver tissues. We found no significant differences in the frequency of losses with regard to tumor size, degree of tumor differentiation, histological degree of tumor spread, or hepatitis B or C infection, although the frequency of losses was higher in cases with portal vein invasion, tumor capsule infiltration, or intrahepatic metastasis. We surmise that the deletion is specific to some HCC, that it occurs through progression, and that it affects the nature of the tumor.

Key words: loss of heterozygosity (LOH), hepatocellular carcinoma (HCC), chromosome 16,
haptoglobin, tumor suppressor gene




本文は、編集委員会の意向によりインターネットには公開しておりません。図書館等でご覧ください。

Texts are not availavle on Internet.



目次・Contentsに戻る